Novel EZH2 mutation in a patient with secondary B-cell acute lymphocytic leukemia after deletion 5q myelodysplastic syndrome treated with lenalidomide: A case report

Medicine (Baltimore). 2019 Jan;98(1):e14011. doi: 10.1097/MD.0000000000014011.

Abstract

Rationale: The gene deletion (5)(q22q35) is reported in 10-20% of myelodysplastic syndrome (MDS) cases and is associated with response to lenalidomide and favorable prognosis. The authors report here a clinical case of MDS transformation to B-cell acute lymphocytic leukemia (B-ALL) with an associated accrual of an additional mutation following treatment with lenalidomide.

Patient concerns: A 69-year-old man presented with progressive anemia, normal white blood cell count, and thrombocytopenia consistent with MDS. He was administered lenalidomide for 27 months, then developed acute B-cell lymphocytic leukemia and acquired a previously unreported mutation in the gene enhancer of zeste homolog 2 (EZH2).

Diagnoses: After 27 months of therapy with lenalidomide, a surveillance bone marrow aspiration (BMA) revealed 90% cellularity with persistent multilineage dysplasia and a population of blasts comprising 54% of all bone marrow elements by morphology, consistent with B-ALL, even though the patient was asymptomatic. Conventional karyotype showed no signs of del(5)(q22q35) MDS, however bone marrow next-generation sequencing (NGS) demonstrated the accrual of a nonsense mutation (c.211del pL71*) in exon 3 of EZH2. A confirmatory BMA yielded 70% blasts and clinical features indicative of B-ALL.

Interventions: Mini-hyper-CVD (cyclophosphamide and dexamethasone at 50% dose reduction, no anthracycline, methotrexate at 75% dose reduction, cytarabine at 0.5 g/m × 4 doses) was administered for 21 days.

Outcomes: A follow-up BMA was performed 2 months after mini-hyper-CVD therapy, showing dysplastic features with 25% ring sideroblasts, but no evidence of B-ALL. The patient is currently receiving monthly-low dose decitabine, ofatumumab, and dexamethasone, and is transfusion independent and asymptomatic after 7 cycles.

Lessons: The present study shows an extremely rare progression of del(5)(q22q35) MDS to B-ALL with accompanying NGS data and a newly described acquisition of an EZH2 frameshift mutation. This case highlights the importance of NGS as a diagnostic and surveillance tool for MDS.

Publication types

  • Case Reports

MeSH terms

  • Aged
  • Anemia / complications
  • Angiogenesis Inhibitors / therapeutic use
  • Antineoplastic Agents, Alkylating / therapeutic use
  • Antineoplastic Agents, Hormonal / therapeutic use
  • B-Lymphocytes / pathology*
  • Bone Marrow / pathology
  • Chromosome Deletion
  • Cyclophosphamide / administration & dosage
  • Cyclophosphamide / therapeutic use
  • Dexamethasone / administration & dosage
  • Dexamethasone / therapeutic use
  • Disease Progression
  • Enhancer of Zeste Homolog 2 Protein / genetics*
  • Humans
  • Lenalidomide / administration & dosage
  • Lenalidomide / therapeutic use
  • Male
  • Mutation
  • Myelodysplastic Syndromes / complications
  • Myelodysplastic Syndromes / drug therapy
  • Myelodysplastic Syndromes / genetics*
  • Myelodysplastic Syndromes / pathology
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics*
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • Thrombocytopenia / complications
  • Treatment Outcome

Substances

  • Angiogenesis Inhibitors
  • Antineoplastic Agents, Alkylating
  • Antineoplastic Agents, Hormonal
  • Dexamethasone
  • Cyclophosphamide
  • EZH2 protein, human
  • Enhancer of Zeste Homolog 2 Protein
  • Lenalidomide